Identification of 1-Methylnicotinamide as a specific biomarker for the progression of cirrhosis to hepatocellular carcinoma.

Purpose: Hepatocellular carcinoma (HCC) is a prevalent malignant tumor, often arising from hepatitis induced by the hepatitis B virus (HBV) in China. However, effective biomarkers for early diagnosis are lacking, leading to a 5-year overall survival rate of less than 20% among patients with advanced HCC. This study aims to identify serum biomarkers for early HCC diagnosis to enhance patient survival rates.

TFIP11 promotes replication fork reversal to preserve genome stability.

Replication fork reversal, a critical protective mechanism against replication stress in higher eukaryotic cells, is orchestrated via a series of coordinated enzymatic reactions. The Bloom syndrome gene product, BLM, a member of the highly conserved RecQ helicase family, is implicated in this process, yet its precise regulation and role remain poorly understood. In this study, we demonstrate that the GCFC domain-containing protein TFIP11 forms a complex with the BLM helicase.

Correlation analysis of cardiopulmonary exercise test indices and conditions of overweight patients with obstructive sleep apnea: a retrospective study.

Background: The cardiopulmonary function of patients with obstructive sleep apnea (OSA) is significantly lower than that of patients with simple snoring and is significantly related to the severity of OSA. Currently, only a few studies have been conducted on cardiopulmonary exercise testing in overweight patients with OSA.

Objective: To analyze the correlation between cardiopulmonary exercise test (CPET) indices and the condition of overweight patients with OSA.

Hypertension as an independent risk factor for severity and mortality in patients with COVID-19: a retrospective study.

Purpose Of The Study: Hypertension is one of the most common comorbidities in COVID-19 pneumonia. However, whether it is an independent factor on the severity and mortality of COVID-19 has not been studied.

Study Design: In this study, 736 patients with a PCR-confirmed diagnosis of COVID-19 were included from 12 January 2020 to 25 March 2020.

BRCA2 antagonizes classical and alternative nonhomologous end-joining to prevent gross genomic instability.

BRCA2-deficient cells exhibit gross genomic instability, but the underlying mechanisms are not fully understood. Here we report that inactivation of BRCA2 but not RAD51 destabilizes RPA-coated single-stranded DNA (ssDNA) structures at resected DNA double-strand breaks (DSBs) and greatly enhances the frequency of nuclear fragmentation following cell exposure to DNA damage. Importantly, these BRCA2-associated deficits are fueled by the aberrant activation of classical (c)- and alternative (alt)- nonhomologous end-joining (NHEJ), and rely on the well-defined DNA damage signaling pathway involving the pro-c-NHEJ factor 53BP1 and its downstream effector RIF1.